The objective of these studies is to define the role of the sympathetic nervous system in respect to ovarian steroid production and to determine if this type of control is lined to the adenyl cyclase -guanyl cyclase systems. Our previous results have shown that an ovarian adenylate cyclase system was activated by beta adrenergic stimulation. Since the effect of LH on steroid production is thought to be mediated by cyclic AMP, it was important to determine if beta adrenergic stimulation could promote steroid production and if separate receptor mechanisms were responsible for the LH- and adrenergic-mediated effects. The following results were obtained using incubated rat ovarian tissue and cell preparations: 1. Isoproterenol and epinephrine increased progesterone production in a dose-related manner (10-7-10-4M) after 2 hours of incubation using preparations of luteal tissue and isolated luteal cells. 2. The addition of a beta adrenergic blocking agent, propranolol, significantly inhibited the effect of the adrenergic agents; however, the blocker did not alter the effect of LH on progesterone production. 3. The addition of isoproterenol to incubations of isolated luteal cells increased cyclic AMP production within 2 min. This effect was also prevented by preincubation in the presence of propranolol. No effect of isoproterenol on cyclic GMP was observed. These results suggest that adrenergic stimulation can promote steroid production by the ovary and provide evidence that these agents are acting directly on ovarian steroid-producing cells. They further support our results suggesting that the effect is linked to the activation of adenylate cyclase and that separate receptor mechanisms are responsible for LH- and adrenergic-mediated effects.